In a murine leukemia model driven by MLL‐AF9 fusion oncogene, Srsf2P95H/+ leukemias were more sensitive to E7107 than Srsf2+/+ wildtype leukemias.31 Similarly, increased sensitivity to spliceosome inhibitors were also observed in Sf3b1K700E/+ and U2af1S34F/+ murine hematopoietic cells in vivo,67, 92 and in SRSF2‐mutant CMML patient‐derived xenograft model.32 These studies provided proof‐of‐concept that a therapeutic window might exist for SF3B inhibitors to achieve the requisite splicing inhibition to selectively kill spliceosomal mutant cells. Here, KMT2A is linked to leukemia.